Category Ranking
98%
Total Visits
921
Avg Visit Duration
2 minutes
Citations
20
Article Abstract
Notch signaling is crucial to animal development and homeostasis. Notch triggers the transcription of its target genes, which produce diverse outcomes depending on context. The high resolution and spatially precise assessment of Notch-dependent transcription is essential for understanding how Notch operates normally in its native context in vivo and how Notch defects lead to pathogenesis. Here we present biological and computational methods to assess Notch-dependent transcriptional activation in stem cells within their niche, focusing on germline stem cells in the nematode Caenorhabditis elegans. Specifically, we describe visualization of single RNAs in fixed gonads using single-molecule RNA fluorescence in situ hybridization (smFISH), live imaging of transcriptional bursting in the intact organism using the MS2 system, and custom-made MATLAB codes, implementing new image processing algorithms to capture the spatiotemporal patterns of Notch-dependent transcriptional activation. These methods allow a powerful analysis of in vivo transcriptional activation and its dynamics in a whole tissue. Our methods can be adapted to essentially any tissue or cell type for any transcript.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1007/978-1-0716-2201-8_11 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Caseinolytic Protease P: A Therapeutic Nexus in Infection, Inflammation, and Immunity.
Crit Rev Immunol
January 2025
Department of Pharmacy, Birla Institute of Technology and Science (BITS) Pilani, Hyderabad Campus, Dist. Medchal,500078, Telangana State, India.
Caseinolytic protease P (ClpP) is a highly conserved serine protease that plays a pivotal role in protein homeostasis and quality control in bacteria, mitochondria of mammalian cells, and plant chloroplasts. As the proteolytic core of the ATP-dependent Clp protease complex, ClpP partners with regulatory ATPases (e.g.
View Article and Find Full Text PDFExtracellular Matrix and Fibroblast Activation in Lymphangioleiomyomatosis.
Am J Respir Cell Mol Biol
September 2025
Univ. of Pennsylvania, Medicine, Philadelphia, Pennsylvania, United States.
Lymphangioleiomyomatosis (LAM) is a rare lung disease caused by hyperactivation of the mechanistic/mammalian target of rapamycin 1 (mTORC1) growth pathway in a subset of mesenchymal lung cells. Histopathologically, LAM lesions have been described as immature smooth muscle-like cells positive for the immature melanocytic marker HMB45/PMEL/gp100 and phosphorylated ribosomal protein S6 (pS6). Advances in single cell sequencing (scRNA-seq) technology allowed us to group LAM cells according to their expression of cancer stem cell (CSC) genes and identify three clusters: a high CSC-like state (SLS), an intermediate state, and a low CSC-like inflammatory state (IS).
View Article and Find Full Text PDFCUX1 restrains latent hematopoietic stem cell plasticity by suppressing stem cell-intrinsic inflammatory pathways.
Blood
September 2025
The University of Chicago, Chicago, Illinois, United States.
Long-term maintenance of somatic stem cells relies on precise regulation of self-renewal and differentiation. Understanding the molecular framework for these homeostatic processes is essential for improved cellular therapies and treatment of myeloid neoplasms. CUX1 is a widely expressed, dosage-sensitive transcription factor crucial in development and frequently deleted in myeloid neoplasia in the context of -7/(del7q).
View Article and Find Full Text PDFCondensation of the Golgi Apparatus Activates YAP1 to Promote Gastric Cancer Progression.
Cancer Res
September 2025
The Catholic University of Korea College of Medicine, Seoul, Korea (South), Republic of.
Alterations in the structure of the Golgi apparatus play a pivotal role in cancer progression and invasion. A better understanding of how Golgi morphology regulates the metastatic potential of cancer cells could help identify potential treatment strategies. In this study, we investigated how specific structural variations in the Golgi, particularly fragmentation and condensation, influence the malignancy of gastric cancer using human cell lines, xenograft mouse models, and human patient tissue samples.
View Article and Find Full Text PDFA Low Sodium Diet Activates HSD2 Neurons in the Nucleus Tractus Solitarii to Promote Sodium Appetite Via the cAMP/MAPK Signaling Pathway.
J Integr Neurosci
August 2025
Department of Neurobiology, Hebei Medical University, 050017 Shijiazhuang, Hebei, China.
Background: Sodium homeostasis is crucial for physiological balance, yet the neurobiological mechanisms underlying sodium appetite remain incompletely understood. The nucleus tractus solitarii (NTS) integrates visceral signals to regulate feeding behaviors, including sodium intake. This study investigated the role of 11β-hydroxysteroid dehydrogenase type 2 (HSD2)-expressing neurons in the NTS in mediating sodium appetite under low-sodium diet (LSD) conditions and elucidated the molecular pathways involved, particularly the cyclic adenosine monophosphate (cAMP)/mitogen-activated protein kinase (MAPK) signaling cascade.
View Article and Find Full Text PDF